Latest / Understanding the Brain / DISCUSSING NOREPINEPHRINE, GABA, GLUTAMATE, AND MORE

Transcript

DISCUSSING NOREPINEPHRINE, GABA, GLUTAMATE, AND MORE · Understanding the Brain

• 0:07
  Speaker 1: Today we're gonna be looking at the other four neurotransmitters.
• 0:12
  Speaker 1: We have a mic now, so hopefully this will sound
• 0:14
  Speaker 1: a little bit better in equality. For West. First we're
• 0:17
  Speaker 1: gona look at is nora perenephrin also known as nora adrenaline,
• 0:21
  Speaker 1: and is based in the locus corolius. That's locus is
• 0:25
  Speaker 1: l O c u S. Corolius is c o E
• 0:29
  Speaker 1: r u E. I'm sorry, c O E r u
• 0:32
  Speaker 1: l e u s in the ponds p o n
• 0:35
  Speaker 1: s and plays a key role in your fight or
• 0:38
  Speaker 1: flight response. So Nora penephrine fight or flight, but its
• 0:43
  Speaker 1: everyday function is more subtle. It fine tunes attention, vigilance
• 0:47
  Speaker 1: and wakefulness. So again it fine tunes attention, vigilance and wakefulness.
• 0:53
  Speaker 1: So if you think about it, lopepherne, what happens fatigue,
• 0:58
  Speaker 1: poor concentration, lower energy. Think of what psychiatric disorder that
• 1:01
  Speaker 1: could be associated with depression? High no apefferent is the
• 1:05
  Speaker 1: opposite agitation, hyper arousal. Think of mania. So maybe you
• 1:09
  Speaker 1: can see bipolar here. I don't know if nouropenefferent fluctuates
• 1:12
  Speaker 1: like that for bipolar, but we see in the mania
• 1:14
  Speaker 1: and anxiety but we also see them being targeted in ADHD. Right,
• 1:20
  Speaker 1: So you have things like atomoxetine stratera that will is
• 1:24
  Speaker 1: a norif nefrin reuptake inhibitor, allowing more nouropenefferne to stay
• 1:28
  Speaker 1: in the synapse to allow you to be more alert
• 1:33
  Speaker 1: and remember. Any kind of ADHD medication like atomoxetine, retolin
• 1:39
  Speaker 1: or aderall they help everybody to improve their attention. This
• 1:42
  Speaker 1: is why it's being abused a lot by college children
• 1:45
  Speaker 1: or college students. Once released, nora upeneffrin binds to alpha
• 1:50
  Speaker 1: and beta adronergic receptors, so these receptors are for adrenaline
• 1:56
  Speaker 1: or no effern similar to dopamine serotonin. It's taken back
• 2:00
  Speaker 1: up or broken down by NAO. The enzymes. Tricyclic antidepressants
• 2:04
  Speaker 1: TCAs like nor tripolen work by blocking the reuptake of
• 2:07
  Speaker 1: both serotonin and more ifnefferent so TCAs. The antidepressants are
• 2:12
  Speaker 1: much stronger than SSRIs and are not used very commonly
• 2:15
  Speaker 1: anymore unless the individual is not getting any success with
• 2:18
  Speaker 1: the SSRIs or SNRIs. We hit over an nowt of
• 2:22
  Speaker 1: gabba in gaba, We're going to wear it up with
• 2:26
  Speaker 1: glutamate you'll see why in a minute. Glutamate is the
• 2:31
  Speaker 1: most excitatory neurotransmitter. So you think about it, Glutamate is
• 2:37
  Speaker 1: the gas pedal, while gabba is the break, right, it's
• 2:39
  Speaker 1: the primary inhibitory neurotransmitter. That's what GABA is, the primary
• 2:44
  Speaker 1: inhibitory neurotransmitter, calming neuronal activity and preventing overstimulation. Oddly enough,
• 2:51
  Speaker 1: GABBA is actually synthesized from glutamate using the enzyme gad low. GABBA.
• 2:56
  Speaker 1: What is it associated with? Well, generalized anxiety disorder, panic attacks, seizures.
• 3:03
  Speaker 1: So you take things like diazepines for instance, like lurazepam
• 3:07
  Speaker 1: which is adavan or valume diazepam, and they work by
• 3:13
  Speaker 1: enhancing GABA a receptor activity, so increasing inhibition and producing sedation, right,
• 3:18
  Speaker 1: calming things down, muscle relaxation, reduced anxiety. But of course
• 3:22
  Speaker 1: with benzos we know tolerance and dependents are major concerns.
• 3:26
  Speaker 1: Highly addictive. GABA does not get reabsorbed like the melanomines. Instead,
• 3:31
  Speaker 1: it's broken down by a gabba transaminase, another target for
• 3:35
  Speaker 1: seizure medications. So the GABBA transaminase is in the enzyme.
• 3:39
  Speaker 1: Anytime you see ase at the end of a word.
• 3:42
  Speaker 1: That's an enzyme. So let's head over to glutamate, which
• 3:47
  Speaker 1: is everywhere. Honestly, it's everywhere in our system. It's over
• 3:51
  Speaker 1: ninety percent of our excitatory synapses in the brain. Use
• 3:56
  Speaker 1: it powers learning, memory and synaptic classicity, especially in the
• 4:00
  Speaker 1: hippocampus and cortex. And it makes sense. Think about it.
• 4:03
  Speaker 1: When you learn, when you add a new memory, when
• 4:06
  Speaker 1: you grew new neurons with synaptic plasticity, that requires energy
• 4:10
  Speaker 1: and work. So it doesn't surprise me that glutamate, the
• 4:14
  Speaker 1: excitatory one, is going to be there. It's got to
• 4:16
  Speaker 1: activate these things, and this is where you use up
• 4:18
  Speaker 1: a lot of energy. It binds that several different receptors
• 4:22
  Speaker 1: NMDA receptors which are involved in long term potentiation, which
• 4:27
  Speaker 1: is the mechanism behind learning. Right, long term potentiation, I
• 4:30
  Speaker 1: want to keep it in my long term memory in
• 4:32
  Speaker 1: the hippocampus. Short term memory is over in the pre
• 4:35
  Speaker 1: funnel cortex. Also the AMPA receptors for fast synaptic transmission
• 4:40
  Speaker 1: and knate kai NATE receptors for modulating signals. So AMPA
• 4:47
  Speaker 1: receptors for fast synaptic transmission and k and A receptors
• 4:51
  Speaker 1: for modulating signals. Too much glutamate causes what they call
• 4:56
  Speaker 1: exo excytosisicity excitote toxicity is a problem. It's when neurons
• 5:03
  Speaker 1: firing themselves to death, so over use in a sense, right,
• 5:07
  Speaker 1: too much excitement, and then they die off. This happens
• 5:10
  Speaker 1: unfortunately in stroke TBIs and even Alzheimer's. So sometimes what
• 5:15
  Speaker 1: they'll do they'll use medications to reduce the damage that
• 5:19
  Speaker 1: can be seen in dementia, like memantine mem A N
• 5:23
  Speaker 1: T I n E to block NMDA receptors. So again
• 5:26
  Speaker 1: they'll use medications like mamantine. Remember, Alzheimer's is a version
• 5:30
  Speaker 1: of dementia. The other version is vascular dementia. So too
• 5:35
  Speaker 1: much glutamate excitotoxicity. So we'll move on to the last
• 5:41
  Speaker 1: one of the neurotransmitters, and then we'll get to neuropeptides.
• 5:44
  Speaker 1: To wrap it up. Seedocholine. It's memory motor control in Alzheimer's.
• 5:50
  Speaker 1: Alzheimer's seedal colin is es central to learning and memory.
• 5:54
  Speaker 1: The acronym for or the abbreviation for acetocholine the ACH
• 5:59
  Speaker 1: and it's decline as a hallmark of Alzheimer's disease. It's
• 6:03
  Speaker 1: made from coline and acetyl CoA and release widely in
• 6:06
  Speaker 1: the cortex and hippocampus as well as neuromuscular junctions for
• 6:10
  Speaker 1: voluntary muscle movements. So let me explain this in a
• 6:13
  Speaker 1: different way. Loss of pol energic neurons, cholinergic neurons, and
• 6:18
  Speaker 1: neurons associated with coline equals a memory deficit in dementia.
• 6:24
  Speaker 1: You may take a medication which is commonly known like
• 6:27
  Speaker 1: aerocept also known as dnapezil. They work by blocking acetyl
• 6:32
  Speaker 1: colon esterase scetyl colon estates. Remember the ase at the end.
• 6:36
  Speaker 1: That means it's an enzyme, so it's blocking that enzyme
• 6:38
  Speaker 1: from breaking it down. That's what enzymes do. So this
• 6:44
  Speaker 1: increases the availability of the acetylcholine and the periphery. Acch
• 6:47
  Speaker 1: plays a role in atomic, nonomic, nervous system function, salivation, digestion,
• 6:53
  Speaker 1: heart rate. Unfortunately, there's nothing now that we can do
• 6:56
  Speaker 1: to stop or reverse dementia. All we can do is
• 7:00
  Speaker 1: mitigate it, and this is what they're trying to do
• 7:02
  Speaker 1: with the aeroceps. So don't be confused as it does
• 7:05
  Speaker 1: not cure Alzheimer's or dementia. It does not reverse it.
• 7:09
  Speaker 1: It just really slows it down in this issue with acetylcholine. Last,
• 7:15
  Speaker 1: but not least is neuropeptides, and they're slower acting, longer
• 7:19
  Speaker 1: lasting molecules, and modulate rather than directly excite or inhibit.
• 7:25
  Speaker 1: So they travel alongside traditional neurotransmitters and they affect mood, pain,
• 7:29
  Speaker 1: and interpersonal bonding. Endorphins bodies natural opioids are an example
• 7:34
  Speaker 1: of them. They reduce pain, enhance pleasure, and released during trauma,
• 7:39
  Speaker 1: intense exercise, or laughter. This is one of the reasons
• 7:42
  Speaker 1: we can relax or reduce the pain, enhance our pleasure.
• 7:47
  Speaker 1: Substance key is involved in transmitting pain signals to the
• 7:51
  Speaker 1: brain oxytocin and vacal press and crucial for attachment, trust,
• 7:56
  Speaker 1: and social bonding studied in autism and trauma. These aren't
• 8:01
  Speaker 1: the first line targets of psychiatric medication, but they do
• 8:04
  Speaker 1: shape how people feel in deep ways, especially embodied ways.
• 8:07
  Speaker 1: Something to remember when exploring trauma, chronic pain, or relational disorders.
• 8:15
  Speaker 1: We'll take a little deeper dive into this now and
• 8:17
  Speaker 1: look at it. So neuropeptides again small protein like molecules
• 8:21
  Speaker 1: that are produced by neurons, and they ride along with them,
• 8:24
  Speaker 1: I guess you can say. So let's look how they
• 8:27
  Speaker 1: affect the psychologically. Neuropeptides such as oxytocin, vasopressin, and endorphins
• 8:33
  Speaker 1: act as neuromodulators. We talked about that many of the
• 8:36
  Speaker 1: neuropeptides interact with the HPA, the hypothalmic p territory adenal axis,
• 8:41
  Speaker 1: regulating stress responses, which of course impact mood and anxiety levels.
• 8:45
  Speaker 1: Gene expression can influence long term changes in brain function
• 8:49
  Speaker 1: by affecting gene expressions. That's what neuropeptides can do as well.
• 8:52
  Speaker 1: They bind to what they call specific G protein coupled
• 8:55
  Speaker 1: receptors where they go trigger cascades that influence neuronal excitability,
• 9:01
  Speaker 1: emotional regulation, and so forth. So let's see how they
• 9:05
  Speaker 1: affect psychiatric conditions. So, depression will have low levels of
• 9:09
  Speaker 1: oxytocin or endorphins, which are associated with depressive symptoms. CRF
• 9:15
  Speaker 1: hyperactivities linked also to chronic stress and major depressive disorder,
• 9:20
  Speaker 1: and that's cortico trope and releasing factor. In addition to that,
• 9:25
  Speaker 1: elevated CRF and neuropeptide y NPY and balances are tied
• 9:30
  Speaker 1: to heightened anxiety and panic disorders. Npy in particularly has
• 9:34
  Speaker 1: a protective role and schizophrenia. Altered levels of CCK and
• 9:40
  Speaker 1: somatostatin are found in schizophrenia, particularly affecting dopamine regulation. Addiction,
• 9:46
  Speaker 1: you'll see edorphin, endorphins and dinorphins influence reward and withdrawal processes,
• 9:52
  Speaker 1: contributing to substance use disorders Autism spectrum disorder. Oxytocin dysregulation
• 9:58
  Speaker 1: is linked to social deficits in autism spectrum disorder, with
• 10:03
  Speaker 1: some studies exploring oxytocin administration as a potential therapeutic option PTSD. Again,
• 10:11
  Speaker 1: an MPY imbalance contributing to hyper arousal, so oxytocin therapy
• 10:20
  Speaker 1: is one thing they're looking at. Neuropyptide y enhancing the
• 10:23
  Speaker 1: NPY signal is being studied for its angeolytic and stress
• 10:27
  Speaker 1: resilience effects. Neuropeptides are complex, with effects varying by brain region,
• 10:32
  Speaker 1: receptor type, and even individual differences. The blood brain barrier,
• 10:36
  Speaker 1: penetration limits drug development. Overstimulation or inhibition of neuropeptide systems
• 10:42
  Speaker 1: can lead to unintended side effects as well, requiring precise targeting.
• 10:47
  Speaker 1: So again those are neuropeptides a little bit more complicated.
• 10:51
  Speaker 1: We saw the other neurotransmitters that will be covered them
• 10:55
  Speaker 1: again GABBA, lutamate and acelocholine and nora epinephern so nor
• 11:01
  Speaker 1: epineffern fight or flight, attention, vigilance, wakefulness associated with major
• 11:07
  Speaker 1: depressive disorder depression with low epinephrine, also associated with mania
• 11:11
  Speaker 1: and anxiety with high neuropinephrine. Use The lots being targeted
• 11:15
  Speaker 1: in ADHD with it's fritera, demoxetine, GABA inhibition and anxiety control, glutamate, memory, learning,
• 11:22
  Speaker 1: and exo excito toxicity. Remember with GABBA, it's associated with
• 11:28
  Speaker 1: generalized anxiety sort of panic attacks over here and glutamate
• 11:34
  Speaker 1: over excitement of it can lead to Alzheimer's disease traumatic
• 11:38
  Speaker 1: brain injury. Medications associated with it are memantine acetacholine. You're
• 11:44
  Speaker 1: looking at learning and memory. It's an early hallmark of
• 11:47
  Speaker 1: Alzheimer's disease for decline, a loss of calinergic neurons. That's
• 11:53
  Speaker 1: what's affecting the memory deficits and dementia. Medications associated or
• 11:56
  Speaker 1: aircept neuropeptides and dwarf friends substance p oxytocin and vas
• 12:02
  Speaker 1: oppressing and that's it. Next time when we meet, we're
• 12:06
  Speaker 1: going to go into the endocrine system and psychological functioning.
• 12:09
  Speaker 1: So hopefully you're enjoying this podcast, I'm really helping you
• 12:14
  Speaker 1: to study better for your E triple P